P-23 PORTAL VEIN THROMBOSIS IS ASSOCIATED WITH HEPATIC DECOMPENSATIONS WITHOUT LIVER STIFFNESS INCREASE IN HEPATOSPLENIC SCHISTOSOMIASIS

No Hepatosplenic schistosomiasis (HSS) is one of the main causes of non-cirrhotic presinusoidal portal hypertension. Although liver stiffness in HSS is typically lower than in cirrhosis, it is still unknown if over the years liver injury related to periportal fibrosis, to metabolic disease or vascular complications can alter liver stiffness and impact in serious hepatic events. This study aims to determine whether metabolic factors, portal vein thrombosis (PVT), or changes in liver stiffness over time are associated with serious hepatic events (SHE) in HSS patients. In this prospective study, adults with laboratory and radiologically confirmed HSS, without concurrent cirrhosis or other liver diseases, were included. All participants underwent initial transient elastography, followed by a second assessment after at least 3 years. The primary outcome was the occurrence of SHE, defined as upper variceal bleeding and/or ascites. Among the 26 patients studied, 65.4% were male, with a mean age of 55 ± 9 years. The main metabolic comorbidities were obesity (27%), hypertriglyceridemia (8%), low HDL-c (4%), and diabetes (13%). Baseline liver stiffness measurement (LSM) was 9.9 kPa (±3.9) and the controlled attenuation parameter (CAP) was 238 dB/m (IQR 121-270). After a median follow-up of 59 months (IQR 51-64), serious hepatic events occurred in 46% of the patients. There was a non-significant median absolute increase in LSM of 1.4 kPa (IQR -1.5 to +3.6) and a median relative increase of +14% (IQR -17% to +50%), with no statistically significant differences in paired analysis (p = 0.140). No metabolic or anthropometric factors were associated with changes in liver stiffness. PVT occurred in 7 patients (26.9%) and was the only factor significantly associated with the occurrence of serious hepatic events (p = 0.026), although it did not significantly interfere with LSM (p = 0.842). LSM remained relatively stable in HSS patients over a median follow-up of almost 5 years, proving to be a useful tool in distinguishing HSS from cirrhosis. SHE were primarily associated with PVT, which may further elevate portal pressure.

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Journal
Annals of Hepatology
Published
2024-12-01
DOI
https://doi.org/10.1016/j.aohep.2024.101637
Primary Topic
Liver Disease and Transplantation
Type
article
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article

P-23 PORTAL VEIN THROMBOSIS IS ASSOCIATED WITH HEPATIC DECOMPENSATIONS WITHOUT LIVER STIFFNESS INCREASE IN HEPATOSPLENIC SCHISTOSOMIASIS

Mateus Jorge Nardelli, Luciana Costa Faria, Carmen Regla Vargas, Cláudia Alves Couto et al.
1 links
Annals of Hepatology
Liver Disease and Transplantation
article

P-23 PORTAL VEIN THROMBOSIS IS ASSOCIATED WITH HEPATIC DECOMPENSATIONS WITHOUT LIVER STIFFNESS INCREASE IN HEPATOSPLENIC SCHISTOSOMIASIS

Mateus Jorge Nardelli, Luciana Costa Faria, Carmen Regla Vargas, Cláudia Alves Couto, Ludmila Resende Guedes, Fernanda Maria Farage Osório, Guilherme Grossi Lopes Cançado, Rafael Theodoro, Guilherme Augusto Lima Figueira
article en

Abstract

No Hepatosplenic schistosomiasis (HSS) is one of the main causes of non-cirrhotic presinusoidal portal hypertension. Although liver stiffness in HSS is typically lower than in cirrhosis, it is still unknown if over the years liver injury related to periportal fibrosis, to metabolic disease or vascular complications can alter liver stiffness and impact in serious hepatic events. This study aims to determine whether metabolic factors, portal vein thrombosis (PVT), or changes in liver stiffness over time are associated with serious hepatic events (SHE) in HSS patients. In this prospective study, adults with laboratory and radiologically confirmed HSS, without concurrent cirrhosis or other liver diseases, were included. All participants underwent initial transient elastography, followed by a second assessment after at least 3 years. The primary outcome was the occurrence of SHE, defined as upper variceal bleeding and/or ascites. Among the 26 patients studied, 65.4% were male, with a mean age of 55 ± 9 years. The main metabolic comorbidities were obesity (27%), hypertriglyceridemia (8%), low HDL-c (4%), and diabetes (13%). Baseline liver stiffness measurement (LSM) was 9.9 kPa (±3.9) and the controlled attenuation parameter (CAP) was 238 dB/m (IQR 121-270). After a median follow-up of 59 months (IQR 51-64), serious hepatic events occurred in 46% of the patients. There was a non-significant median absolute increase in LSM of 1.4 kPa (IQR -1.5 to +3.6) and a median relative increase of +14% (IQR -17% to +50%), with no statistically significant differences in paired analysis (p = 0.140). No metabolic or anthropometric factors were associated with changes in liver stiffness. PVT occurred in 7 patients (26.9%) and was the only factor significantly associated with the occurrence of serious hepatic events (p = 0.026), although it did not significantly interfere with LSM (p = 0.842). LSM remained relatively stable in HSS patients over a median follow-up of almost 5 years, proving to be a useful tool in distinguishing HSS from cirrhosis. SHE were primarily associated with PVT, which may further elevate portal pressure.

Annals of HepatologyVol. 29
Universidade Federal de Minas Gerais (BR)
Zero hunger
Openalex Percentile: Top 65%
Liver Disease and Transplantation
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